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compound 7n  (MultiTarget Pharmaceuticals)

 
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    MultiTarget Pharmaceuticals compound 7n
    Compound 7n, supplied by MultiTarget Pharmaceuticals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/compound+7n/compound+7n/10__3390_slash_molecules25204614-5-0-24
    Average 90 stars, based on 1 article reviews
    compound 7n - by Bioz Stars, 2026-09
    90/100 stars

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    other:

    Article Title: Synthesis, Docking, 3-D-Qsar, and Biological Assays of Novel Indole Derivatives Targeting Serotonin Transporter, Dopamine D2 Receptor, and Mao-A Enzyme: In the Pursuit for Potential Multitarget Directed Ligands
    Article Snippet: Compound 7n was the only derivative displaying comparable affinities for SERT and D2 receptor (D2/SERT ratio = 3.6) and could be considered as a multitarget lead for further optimization.



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    PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound <t>7n</t> and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.
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    compound 7n  (MultiTarget Pharmaceuticals)
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    PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound <t>7n</t> and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.
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    PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound <t>7n</t> and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.
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    PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound <t>7n</t> and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.
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    PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound 7n and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.

    Journal: Journal of Cell Communication and Signaling

    Article Title: JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

    doi: 10.1002/ccs3.12017

    Figure Lengend Snippet: PIK3CD inhibitors suppressed GC cell viability in vitro. (A) Four GC cell lines as indicated were treated with Acalisib, Compound 7n and Idelalisib for 48 h, and then CCK‐8 analysis was performed. IC 50s were determined by GraphPad Prism 7 using the nonlinear regression subprogram. (B) Colony formation assays with GC cells treated with different concentrations of Acalisib, Compound 7n and Idelalisib for 2 weeks. Data are represented as mean ± SD of independent experiments ( n = 3). * p < 0.05, ** p < 0.01. GC, gastric cancer; IC 50s , inhibitory concentrations; SD, standard deviation.

    Article Snippet: PI3Kδ inhibitors, including Acalisib (#S5818), compound 7n (#S8693) and Idelalisib (#S2226), STAT3/STAT5 inhibitor SH‐4‐54 (#S7337), STAT3 inhibitor BP‐1‐102 (#S7769), and JAK3 inhibitor JANEX‐1 (#S5903) were purchased from Selleck Chemicals.

    Techniques: In Vitro, CCK-8 Assay, Standard Deviation